Drugs Employed in GI Disease 1 Flashcards Preview

MS2 Unit 6 Pharm > Drugs Employed in GI Disease 1 > Flashcards

Flashcards in Drugs Employed in GI Disease 1 Deck (25):

the 2 causes for ulcers

increased acid production and decreased mucosal resistance


3 interventions for ulcers

1. neutralize acid
2. decrease acid production
3. increase mucosal resistance


calcium carbonate

antacid. reacts w/ HCl to make calcium chloride and carbonic acid. side effect is constipation. use in combo with magnesium compounds


sodium bicarbonate

antacid. rarely used because of systemic alkalosis. high sodium content


magnesium hydroxide/magnesium carbonate

antacid. may cause magnesium toxicity in presence of renal disease. adverse effects include diarrhea. can cause bradycardia with renal problems.


aluminum hydroxide

antacid. combines with HCl to make aluminum chloride and water. aluminum Cl -> aluminum phosphate which cant be absorbed. doesnt disturb serum electrolyte or pH. useful in renal failure patients. may have protective effect on mucosa. causes constipation



defoaming agent in antacids. decreases gas bubbles/bloating



used with antacids. small amounts, but can cause concern in patients with edema and hypertension.


anticholinergic agents effect

vagotomy type of effect. reduction of HCl secretion, spasmolytic effect. adverse effects include dry mouth, blurry vision, atony of bladder, constipation, drowsiness, confusion.


anticholinergic drugs + when you take them

atropine, propantheline, dicyclomine. administered 30 minutes before meals and at bedtime.


blockade of histamine H2 receptor

lower acid secretion by blocking H2 histamine receptors on parietal cells. decrease basal and food stimulated acid secretion. dont need to be given in relationship to meals


H2 receptor antagonists list

cimetidine, ranitidine, famotidine, nizatidine. inhibi 50-80% of 24 hour acid secretion.


other use for H2 receptor antagonists

can be used prophylactically to decrease stress ulcers in ICU and burn patients.


what happens if you abruptly stop h2 blockers?

hyperproduction of acid! ween off slowly


H2 blocker adverse effects

messes with p450 so can interfere with metabolism of other drugs. headache, lethargy, confusion, depression. severe side effects uncommon


list the 6 H/K ATPase inhibitors (proton pump inhibitors)

omeprazole, lansoprazole, rabeprazole, esomeprazole, pantoprazole, dexlansoprazole


which proton pump inhibitors can be given IV

pantoprazole. doesn't mess with p450.


proton pump inhibitor mechanism of action

accumulate selectively in the highly acid environment of the canniliculus. protonated to a reactive thiophillic sulfenamide that binds to cysteine 813 in the alpha subunit of the enzyme. non competitive inhibitors. better pain relief and faster ulcer healing rates than with H2 antagonists. will heal H2 refractory ulcers


adverse effects of PPIs

headache, gynecomastia, inhibition of P450, gastric hyperplasia possible in long term stuff.


factors impairing mucosal resistance to acid

smoking, genetics, stress, NSAIDs, H. pylori


bismuth salts

in acid environment it forms crystals that precipitate on the ulcer crater. lower ulcer recurrence rate than with h2 antagonists



aluminum hydroxide complex, activates in acid environment, binds to ulcerated tissue. as effective as H2 antagonists.


what type of ulcers are prostaglandin E2 analogs

used in people with NSAID ulcers, because duodenal ulcer patients already hyperproduce E2 prostaglandins



prostaglandin E2 analog. decrease acid production, increase mucous and bicarb secretion. less effective than H2 blockers when used solo. approved for prevention of NSAID ulcers. can cause diarrhea, dont use in pregnant bitches!


preferred therapies for H. pylori infection

twice a day PPI or ranitidine bismuth citrate triple therapies (PPI or bismuth + 2 of antobiotics)

quadruple therapy: PPI twice a day, tetracycline, bismuth, metronidazole